Journal of Bacteriology & Parasitology

Quinolone resistant molecular mechanisms in Escherichia coli isolated from University Hospital in Egypt

7^th World Congress on Microbiology

November 28-29, 2016 Valencia, Spain

Sherine Ahmed Abd El-Rahman Aly

Assiut University, Egypt

Posters & Accepted Abstracts: J Bacteriol Parasitol

Abstract:

Fluorpquinolone resistant E. coli (FQREC) is an important cause of many infectious diseases worldwide. Our goal is to detect the prevalence of FQREC in Egypt in addition to unrevealing the most important molecular mechanisms of FQ resistance. Forty E. coli isolates were tested for their ciprofloxacin MIC by E-test and for mutations in genes coding for DNA Gyrase (gyrA & gyrB), Topoisomerase IV (parC & parE) and transcriptional regulators of AcrAB efflux pump; soxR, soxS, marR and acrR using Polymerase Chain Reaction (PCR) and sequencing. The contribution of PMQR to resistance was based on PCR detection of qnrA, qnrB, qnrS, qnrD, aac(6â??)-lb-cr, and qepA determinants. All FQREC isolate had at least double mutations within gyrA plus a third mutation in parC. Some FQR isolates also manifested an additional mutation either in the parC or in parE. Regarding the AcrAB pump regulators, stop mutations both in soxR and acrR were recorded in addition to silent mutations in marA. Interestingly the A12S mutation in soxS discovered in canine E. coli isolates have been found for the first time in 2 of human isolates of this study. Three of the FQSEC showed decreased susceptibility to ciprofloxacin, one of them harbor a single gyrA mutation and another one showed a stop codon in soxR. qnrS and aac(6â??lb) were the most prominent plasmid found in 13 and 14 FQREC isolates respectively. qnrA. qnrB and qepA were found in fewer isolates. Interestingly, one FQREC isolate harbor all the five plasmids together. Two of the FQSEC isolates with reduced susceptibility contain PMQR.

Biography :

Email: s-aly71@windowslive.com